Pulmonary Edema

Pulmonary Edema

Afterload Reduction

Angiotension-Converting Enzyme (ACE) Inhibitors

Antidysrhythmic Agents

Bat’s Wing x-ray Appearance

Butterfly Pattern

Calcium Channel Blockers

Cardiogenic Pulmonary Edema

Congestive Heart Failure (CHF)

Decompression Pulmonary Edema

Direct-Acting Vasodilators

Increased Capillary Permeability

Indirect-Acting Vasodilators

Kerley A and B Lines

Morphine Sulfate

Noncardiogenic Pulmonary Edema

Oncotic Pressure

Paroxysmal Nocturnal Dyspnea (PND)

Positive Inotropic Agents

Starling’s Equation

Anatomic Alterations of the Lungs

Pulmonary edema results from excessive movement of fluid from the pulmonary vascular system to the extravascular system and air spaces of the lungs. Fluid first seeps into the perivascular and peribronchial interstitial spaces; depending on the degree of severity, fluid may progressively move into the alveoli, bronchioles, and bronchi (see Figure 19-1).

FIGURE 19-1 Pulmonary edema. Cross-sectional view of alveoli and alveolar duct in pulmonary edema. FWS, Frothy white secretions; IE, interstitial edema; RBC, red blood cell. Inset, Atelectasis, a common secondary anatomic alteration of the lungs.

As a consequence of this fluid movement, the alveolar walls and interstitial spaces swell. As the swelling intensifies, the alveolar surface tension increases and causes alveolar shrinkage and atelectasis. Moreover, much of the fluid that accumulates in the tracheobronchial tree is churned into a frothy white (sometimes blood-tinged or pink) sputum as a result of air moving in and out of the lungs. The abundance of fluid in the interstitial spaces causes the lymphatic vessels to widen and the lymph flow to increase.

Pulmonary edema is a restrictive pulmonary disorder. The major pathologic or structural changes of the lungs associated with pulmonary edema are as follows:

• Interstitial edema, including fluid engorgement of the perivascular and peribronchial spaces and the alveolar wall interstitium

• Alveolar flooding

• Increased surface tension of alveolar fluids

• Alveolar shrinkage and atelectasis

• Frothy white (or pink) secretions throughout the tracheobronchial tree

Etiology and Epidemiology

The causes of pulmonary edema can be divided into two major categories: cardiogenic and noncardiogenic.

Cardiogenic Pulmonary Edema

The most common cause of cardiac pulmonary edema is left-sided heart failure—commonly called congestive heart failure (CHF). According to the Centers for Disease Control and Prevention (CDC), about 5 million people in the United States have CHF—or about 1.7% of the overall population. Approximately 550,000 new cases of CHF are diagnosed annually. Heart failure is most common in people over age 65 and is more common in African-Americans. CHF is a leading cause of hospitalization in people over the age of 65 and is estimated to be a contributing factor to nearly 300,000 deaths annually. In 2008 the estimated annual direct and indirect costs associated with heart failure totaled nearly 35 billion dollars. As the median age of the U.S. population of “baby boomers” continues to grow older—between the present and 2040—the number of patients diagnosed with CHF, along with the direct and indirect costs associated with CHF, will undoubtedly continue to rise.

Cardiac pulmonary edema occurs when the left ventricle is not able to pump out all of the blood that it receives from the lungs. As a result, the blood pressure inside the pulmonary veins and capillaries increases. This action literally causes fluid to be pushed through the capillary walls and into the alveoli in the form of a transudate. The basic pathophysiologic mechanism for this action is described in the following sections.

Ordinarily, hydrostatic pressure of about 10 to 15 mm Hg tends to move fluid out of the pulmonary capillaries into the interstitial space. This force is normally offset by colloid osmotic forces of about 25 to 30 mm Hg that tend to keep fluid in the pulmonary capillaries. The colloid osmotic pressure is referred to as oncotic pressure and is produced by the albumin and globulin in the blood. The stability of fluid within the pulmonary capillaries is determined by the balance between hydrostatic and oncotic pressure. This relationship also maintains fluid stability in the interstitial compartments of the lung.

Movement of fluid in and out of the capillaries is expressed by Starling’s equation:

J=K(Pc−Pi)−(πc−πi)

where J is the net fluid movement out of the capillary, K is the capillary permeability factor, Pc and Pi are the hydrostatic pressures in the capillary and interstitial space, and πc and πi are the oncotic pressures in the capillary and interstitial space.

Although conceptually valuable, this equation has limited practical use. Of the four pressures, only the oncotic and hydrostatic pressures of blood in the pulmonary capillaries can be measured with any certainty. The oncotic and hydrostatic pressures within the interstitial compartments cannot be readily determined.

When the hydrostatic pressure within the pulmonary vascular system rises to more than 25 to 30 mm Hg, the oncotic pressure loses its holding force over the fluid within the pulmonary capillaries. Consequently fluid starts to spill into the interstitial and air spaces of the lungs (see Figure 19-1).

Clinically, the patient with left ventricular failure often has anxiety, delirium, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue, and adventitious breath sounds. Because of poor peripheral circulation, such patients often have cool skin, diaphoresis, cyanosis of the digits, and peripheral pallor. Increased pulmonary capillary hydrostatic pressure is the most common cause of pulmonary edema. Box 19-1 provides common causes of cardiogenic pulmonary edema. Box 19-2 provides common risk factors for coronary heart disease (CHD).

Box 19-1 Common Causes of Cardiogenic Pulmonary Edema

• Arrhythmias (e.g., premature ventricular contractions or bradycardia producing low cardiac output)

• Systemic hypertension

• Congenital heart defects

• Excessive fluid administration

• Left ventricular failure

• Mitral or aortic valve disease

• Myocardial infarction

• Cardiac Tamponade

• Pulmonary embolus

• Renal failure

• Rheumatic heart disease (myocarditis)

• Cardiomyopathies (e.g., viral)

Box 19-2 Risk Factors for Coronary Heart Disease (CHD)

Male >45 years old

Female >55 years old

• Family history of CHD

Male relative: <55 years old

Female relative: <65 years old

• Cigarette smoker

• Hypertension: (blood pressure >140/90 mm Hg or on antihypertensive agents)

• High level of low-density–lipoprotein cholesterol (LDL-C): >130 mg/dL (“bad cholesterol”)

• Low level of high-density–lipoprotein cholesterol (HDL-C): <35 mg/dL (“good cholesterol”)

• High level of homocysteine: >10 mg/dL

• High total cholesterol level (>150-200 mg/dL) and high triglyceride level (>200-300 mg/dL)

• Diabetes mellitus (type 1 and type 2)

Noncardiogenic Pulmonary Edema

There are numerous noncardiogenic causes of pulmonary edema. In these conditions, fluid can readily flow from the pulmonary capillaries into the alveoli—even in the absence of the back pressure caused by an abnormal heart. The more common conditions include those discussed in the following paragraphs.

Increased Capillary Permeability

Pulmonary edema may develop as a result of increased capillary permeability stemming from infectious, inflammatory, and other processes. The following are some causes of increased capillary permeability:

• Alveolar hypoxia

• Acute respiratory distress syndrome (ARDS)

• Inhalation of toxic agents such as chlorine, sulfur dioxide, nitrogen dioxides, ammonia, and phosgene

• Pulmonary infections (e.g., pneumonia)

• Therapeutic radiation of the lungs

• Acute head injury (also known as cephalogenic pulmonary edema)

Lymphatic Insufficiency

Should the lungs’ normal lymphatic drainage be decreased, intravascular and extravascular fluid begins to pool, and pulmonary edema ensues. Lymphatic drainage may be slowed because of obliteration or distortion of lymphatic vessels. The lymphatic vessels may be obstructed by tumor cells in lymphangitic carcinomatosis. Because the lymphatic vessels empty into systemic veins, increased systemic venous pressure may slow lymphatic drainage. Lymphatic insufficiency also has been observed after lung transplantation.

Decreased Intrapleural Pressure

Reduced intrapleural pressure may cause pulmonary edema. With severe airway obstruction, for example, the negative pressure exerted by the patient during inspiration may create a suction effect on the pulmonary capillaries and cause fluid to move into the alveoli. Furthermore, the increased negative intrapleural pressure promotes filling of the right side of the heart and hinders blood flow in the left side of the heart. This condition may cause pooling of the blood in the lungs and subsequently an elevated hydrostatic pressure and pulmonary edema. A related kind of pulmonary edema is caused by the sudden removal of a pleural effusion. Clinically this condition is called decompression pulmonary edema.

Decreased Oncotic Pressure

Although this condition is rare, if the oncotic pressure is reduced from its normal 25 to 30 mm Hg and falls below the patient’s normal hydrostatic pressure of 10 to 15 mm Hg, fluid may begin to seep into the interstitial and air spaces of the lungs. Decreased oncotic pressure may be caused by the following:

• Overtransfusion and/or rapid transfusion of intravenous fluids

• Hypoproteinemia (e.g., severe malnutrition)

• Acute nephritis

• Polyarteritis nodosa

Although the exact mechanisms are not known, Box 19-3

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Tags: Clinical Manifestations _ Assessment of Respiratory Disease

Jun 11, 2016 | Posted by admin in RESPIRATORY | Comments Off

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